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PubMed1982

Electron microscopic demonstration of neural connections using horseradish peroxidase: a comparison of the tetramethylbenzidine procedure with seven other histochemical methods.

Eight methods for the electron microscopic demonstration of horseradish peroxidase (HRP) labeling have been compared in adjacent series of vibratome sections of mouse lumbar spinal cord. The tracer, a HRP-wheat germ agglutinin (WGA) conjugate, was injected into the gastrocnemius muscle complex. Following retrograde axonal transport to the lumbar motor neurons and transganglionic anterograde transport of the tracer to the dorsal horn, the HRP activity was demonstrated in eight series of adjacent sections of lumbar spinal cord using eight methods. These included procedures using tetramethylbenzidine (TMB), benzidine dihydrochloride (BDHC), o-tolidine, paraphenylenediamine-pyrocatechol (PPD-PC), and 4 methods using 3,3'-diaminobenzidine (DAB). All eight methods were able to demonstrate both retrograde labeling of motor neurons and transganglionic anterograde transport into the dorsal horn. However, there were differences in the appearance of the various reaction products under the electron microscope. In addition, differences in the distribution of the reaction products were observed by both light and electron microscopy. The largest distribution of reaction product was observed with TMB. BDHC and o-tolidine were next, followed by the DAB procedures and PPD-PC. The TMB, BDHC, and o-tolidine reaction products were all found to be suitable for electron microscopy. The TMB reaction product was electron dense and had a very distinctive crystalloid appearance that made identification of HRP-labeled neuronal profiles easy and unequivocal.

Animals↗
PubMed1989

A double-label pre-embedding immunoperoxidase technique for electron microscopy using diaminobenzidine and tetramethylbenzidine as markers.

Techniques for correlative double-label immunocytochemistry (ICC) at light and electron microscopic (EM) level are useful for determining the neurotransmitter phenotype of inputs onto immunocytochemically identified neurons. Tetramethylbenzidine (TMB) has been used as a chromogen at the EM level for horseradish peroxidase tract tracing. We have found that TMB, in combination with diaminobenzidine (DAB), can be used in a double-label immunocytochemical protocol to examine neuropeptide Y inputs onto luteinizing hormone-releasing hormone cells in the sheep preoptic area. At both light and EM levels, TMB reaction product is visibly distinct from DAB reaction product. The ultrastructural preservation we have been able to obtain with our technique is better than that obtained with techniques that use TMB at a lower pH. Furthermore, this technique allows the demonstration of synaptic contacts between neurochemically identified terminals and cells with different neurotransmitter phenotypes.

3,3'-Diaminobenzidine↗
PubMed1988

Role of calcium in prolactin-stimulated c-myc gene expression and mitogenesis in Nb2 lymphoma cells.

Receptor-activated transmembrane calcium flux has been implicated as a mediator of the actions of many growth factors and hormones. We examined the effects of PRL, calcium ionophores, and calcium antagonists on 45Ca2+ flux, c-myc gene expression, and DNA synthesis in the PRL-dependent rat Nb2 lymphoma cell line. PRL had no detectable effects on 45Ca2+ uptake or efflux, and the mitogenic effects of PRL could not be reproduced by the calcium ionophore A23187 alone or in combination with the tumor-promoting phorbol ester 12-O-tetra-decanoyl-phorbol-13 acetate (TPA). PRL, but not A23187 or TPA, stimulated c-myc gene expression in quiescent Nb2 cells. Exposure to PRL for brief periods (15 min to 4 h), followed by extensive washing, resulted in a time- and dose-dependent activation of DNA synthesis measured 16 h later. This activation was not blocked by addition of excess anti-PRL antiserum after the wash steps, indicating that the observed stimulation was not due to residual PRL. Despite the marked increase in DNA synthesis, removal of PRL after 4 h prevented mitosis, suggesting that PRL may be required throughout the cell cycle for Nb2 cell proliferation. Although continuous incubation with calcium antagonists resulted in a dose-dependent inhibition of PRL-stimulated DNA synthesis, activation of DNA synthesis by brief exposure to PRL was not inhibited by the presence of EGTA, calcium channel blockers (nifedipine, cobalt chloride), or calmodulin inhibitors (trifluoperazine, N-6-aminohexyl-5-chloronaphthalene sulfonamide). PRL-stimulated c-myc expression was attenuated, but not blocked, by the calcium channel antagonists. However, the putative intracellular calcium antagonist TMB-8 inhibited both c-myc expression and DNA synthesis in a dose-dependent manner (IC50 = 16 microM). Nb2 cells were sensitive to TMB-8 throughout G1 of the cell cycle, but inhibition of DNA synthesis was greatest when TMB-8 was present during the first 3 h of mitogen presentation, indicating a block in the transition from G0 to G1 of the cell cycle. The effect of TMB-8 suggests that release of a small intracellular calcium pool may mediate the early actions of PRL in Nb2 cells.

Animals↗
PubMed1991

Ultrastructural evidence for luteinizing hormone-releasing hormone neuronal control of estrogen responsive neurons in the preoptic area.

Both estrogen receptor (ER) immunoreactive (ir) and LHRH-ir neurons and processes are present in the preoptic area of the guinea pig. This experiment was conducted to determine if LHRH-ir terminals interact synaptically with ER-ir cells. A light microscopic dual chromogen immunocytochemical technique employing diaminobenzidine (DAB) and nickel-enhanced DAB for LHRH and ER localization, respectively, revealed that many varicose LHRH-ir fibers coursed in close proximity to ER-ir cells in the anterior part of the preoptic area at the preventricular periventricular nucleus (Pep), suggesting the likelihood of synaptic interactions. Ultrastructural analysis was performed using DAB and 3,3',5,5'-tetramethylbenzidine (TMB) for LHRH and ER localization, respectively. DAB labeling in LHRH-ir neurons appeared as a dense flocculent product dispersed throughout the cytoplasm. TMB stained ER-ir neurons contained electron dense crystalline spicules located predominantly in their nuclei. Numerous TMB labeled ER-ir neurons were present in the Pep, and occasionally occurred in clusters, closely apposed to one another. Many LHRH-ir terminals made synaptic contact or were apposed to unlabeled dendrites, while fewer contacted perikarya. Most significantly, ER-ir neurons showing clear evidence of intranuclear TMB crystals received synaptic input from LHRH-ir terminals. In addition, LHRH-ir terminals lacking synaptic specializations were also in direct apposition to ER-ir perikarya. These results provide morphological evidence that LHRH-ir neurons can regulate ER-ir neurons in the preoptic area. Since LHRH-ir cells are thought to be regulated by estrogen responsive neurons, interaction of LHRH terminals with ER-ir cells may represent a regulatory feedback circuit between the two systems.

3,3'-Diaminobenzidine↗
PubMed1992

Estrogen receptor-immunoreactive glia, endothelia, and ependyma in guinea pig preoptic area and median eminence: electron microscopy.

The presence of estrogen receptors (ERs) in nonneural cells in brain, including glia, ependyma, and endothelia, has not previously been documented with electron microscopy. This study employed immunocytochemistry to investigate whether ER immunoreactivity (ER-ir) is present in glial, ependymal, or endothelial cells in the medial preoptic area (POA) and median eminence (ME) in the brain of gonadally intact female guinea pigs. Tissue sections through these regions were immunostained with monoclonal antibody H222 for ER localization using 3,3',5,5'-tetramethylbenzidine (TMB) as the chromogen. ER-ir cells were identified ultrastructurally by the presence of distinct spicule-like TMB crystals in nuclei. While neurons constituted the clear majority of ER-immunopositive cells, labeled astrocytes, ependyma, and endothelia were also present. Distinct intranuclear TMB crystals were present in astrocytes at the anterior pole of the POA within the preventricular periventricular nucleus, anterior compact subnucleus of the medial preoptic nucleus (MPNa), and organum vasculosum of the lamina terminalis, indicating ER-ir. In the MPNa, cell counts performed at the ultrastructural level revealed that 9.6% (15 of 156) of the astrocytes were ER-ir. To further explore the relationship of ERs with astrocytes, ER/glial fibrillary acidic protein (GFAP) double labeling experiments were performed using TMB and diaminobenzidine tetrahydrochloride for ER and GFAP localization, respectively. These studies verified the presence of ERs in astrocytes at the anterior pole of the POA and demonstrated the presence of ERs in GFAP-ir cells in the ME. Cell counts at the ME showed that 23 of 50 (46%) GFAP-ir cells were ER-ir. ER-ir was also present in scattered ependymal cells lining the third ventricle at the POA and overlying the ME. Typically, approximately four to eight ER-ir ependymal cells were present around the perimeter of the third ventricle, although occasionally small aggregations of greater numbers of labeled cells were observed. Both common ependyma and cells morphologically identified as tanycytes were ER-ir. Some endothelial cells and vascular smooth muscle cells also contained ERs. While approximately 11% of the vessels were lined by ER-ir cells in sections through the MPNa and preventricular periventricular nucleus, approximately 15% of the vessels were labeled in the organum vasculosum of the lamina terminalis. In the ME a greater percentage (59%) of the vessels contained ER-ir endothelial cells. Collectively, these results indicate that in addition to regulating the activity of neurons, estrogen may affect brain function through effects exerted on astrocytes, ependymal cells, and endothelial cells.

Animals↗
PubMed2026

Construction of molecular signatures based on the co-expression network of NECSO-related gene TRPM4 and its prognostic value in hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) demonstrates significant prognostic variability that is not entirely accounted for by traditional staging systems. Necrosis by sodium overload (NECSO) is an emerging programmed cell death pathway, but its clinical relevance in HCC remains undefined. Therefore, this study aimed to identify TRPM4-associated core genes, develop and validate a prognostic signature, and investigate its relationship with the tumor immune microenvironment, tumor mutational burden, and single-cell expression patterns in HCC. METHODS: We integrated transcriptomic, clinical, and mutational datasets from The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) (n=421) and Gene Expression Omnibus (GEO) cohorts (n=115) to identify genes co-expressed with TRPM4-a key NECSO mediator-and those differentially expressed in HCC. A prognostic signature was developed using least absolute shrinkage and selection operator (LASSO)-Cox regression and validated through survival analysis, time-dependent receiver operating characteristic (ROC) curves, and multivariate Cox regression analysis. The immune landscape was characterized using CIBERSORT, somatic mutation data were used to calculate tumor mutational burden (TMB) and assess its correlation with the risk score, and single-cell RNA sequencing (scRNA-seq) resolved cell-type-specific expression patterns. RESULTS: From 294 TRPM4-associated core genes, we identified an 11-gene signature (BRSK1, MMP1, GRIN2D, GP6, MYOM2, N4BP3, CCDC112, TSEN54, MAP3K9, SPP1, B3GNT4) that independently predicted overall survival (OS) (hazard ratio =5.419, P<0.001) with areas under the curve (AUCs) of 0.779, 0.693, and 0.701 at 1, 3, and 5 years. These values were superior or comparable to conventional clinicopathologic variables after direct comparison. High-risk patients exhibited an immunosuppressive microenvironment, characterized by enrichment of M0 macrophage, a higher M2/M1 ratio (P<0.001) and distinct immune checkpoint profiles. When integrated with TMB, the prognostic stratification was further refined: high-TMB/high-risk patients had poorest outcomes (median OS, 15.3 months), while low-TMB/low-risk patients had the most favorable survival (median OS, 68.7 months). Single-cell analysis revealed that MMP1 was induced in cancer-associated fibroblasts (CAFs) and SPP1 was downregulated in macrophages, single-cell risk scores confirmed TAFs and macrophages as the main contributors to the prognostic model. CONCLUSIONS: The TRPM4-centered 11-gene signature provides robust and independent prognostic stratification in HCC by integrating immune, mutational, and single-cell features. This signature serves as a potential tool for prognostic evaluation and may help inform immunotherapeutic strategies for HCC.

Hepatocellular carcinoma (HCC)↗
PubMed2001

Streptococcus iniae inhibition of apoptosis of nonspecific cytotoxic cells: a mechanism of activation of innate immunity in teleosts.

Nonspecific cytotoxic cells (NCC) may provide innate anti-bacterial resistance against Streptococcus iniae infections in tilapia. The mechanism of immunity would be elaboration and release of various cytokines, augmentation of inflammation and amplification of increased antigen processing. To investigate bacterial regulation of NCC function, 2 different processes of cellular pathology were examined: apoptosis and necrosis. Different isolates of S. iniae from diseased teleosts, a dolphin and a human were tested. All isolates were examined for their ability to produce apoptosis and/or necrosis on freshly purified tilapia NCC and on a tilapia continuous cell line (i.e. TMB-8 cells). Two different isolates (9033 and 173) inhibited the outer membrane expression of phosphatidylserine (PS) by NCC, an early sign of apoptosis. This occurred at 4 h post-treatment and lasted throughout the 24 h treatment period. All other isolates either did not differ from control levels or produced a small increase in PS expression by NCC. The early reduction in PS expression occurred concomitantly with increased necrosis associated with nonspecific DNA fragmentation. Two-color flow cytometry (Annexin-V vs propidium iodide staining) demonstrated the specificity of Annexin-V binding. Experiments were also done to determine the effects of S. iniae on TMB-8 cells. Treated TMB-8 cells did not produce appreciable Annexin-V binding. Compared to the ATCC strain, 9033 produced high levels of necrosis-associated DNA fragmentation of TMB-8 cells at 4 and 8 h post-treatment. These data indicated that different isolates of S. iniae may regulate NCC anti-bacterial resistance by causing reduced levels of programmed cell death (PCD), increased necrosis and associated enhancement of inflammatory responses. Understanding the relevance of these bacterial effects on NCC may be an important consideration in the evaluation of isolates used in vaccine/ bacterin production.

Animals↗
PubMed1990

A rapid sporozoite ELISA using 3,3',5,5'-tetramethylbenzidine as the substrate chromogen.

A modified version of the standard 2-site sporozoite enzyme-linked immunosorbent assay (ELISA) using 3,3',5,5'-tetramethylbenzidine (TMB) as the substrate chromogen solution was adapted for rapid detection and identification of Plasmodium falciparum and P. vivax circumsporozoite (CS) proteins. The TMB-ELISA was evaluated using sporozoites from experimentally infected mosquitoes and laboratory colonized uninfected mosquitoes. Our data indicate comparable sensitivity levels between the TMB-ELISA and the standard ELISA, i.e., 50 P. falciparum or P. vivax sporozoites/50 microliters of test solution. Reactions inherent to the method were specific and background reactivity was minimal. The TMB-ELISA is rapid (1 hr), simple, uses a minimal amount of monoclonal antibodies, and is suitable for use in a wide range of laboratories.

Animals↗
PubMed1998

Behavioural changes following a four-week inhalation exposure to hemimellitene (1,2,3-trimethylbenzene) in rats.

Trimethylbenzene isomers (TMBs): 1,2,4-TMB (pseudocumene--PS), 1,2,3-TMB (hemimellitene--HM) and 1,3,5-TMB (mesitylene--MES) are important constituents of solvent mixtures. In the US, the adopted TLV-TWA value for TMBs is 125 mg/m3 or 25 ppm (ACGIH 1996). Recent experiments at our laboratory have revealed an impaired learning of passive and active avoidance responses and a longer persistence of an effect of footshock (increase in latency of the paw-lick response to heat) in rats tested several weeks after a four-week inhalation exposure (6h/day, five days/week) to PS at a concentration of 100 or 250 ppm (15). The concentration-effect relationship appeared to be nonlinear; the effect of 100 ppm HM was more pronounced than that of 250 ppm. In the present experiment we investigated the effects of a repeated four-week (6h/day, 5 days/week) inhalation exposure to HM at concentrations of 0, 25, 100 or 250 ppm on radial-maze performance, open-field activity, passive and active avoidance learning, and on the shock-induced changes in latency of the paw-lick response to heat (hot-plate test). The tests were performed between days 14 and 61 after the last exposure. No significant effects on radial-maze performance and open-field activity were noted in any of the dose groups. In the remaining tests effects of exposure were noted but, similarly as in the case of PS exposure, the concentration-effect relationship was not linear. In rats exposed to HM at 25 or 100 ppm, but not 250 ppm, learning of the passive avoidance, i.e. refraining from performance of a punished response (stepping off an elevated platform) was significantly impaired. Moreover, in rats exposed to 100, but not 250 ppm of HM, acquisition of the two-way active avoidance in the shuttle-box was slower and the footshock-induced increase in latency of the paw-lick response to heat persisted longer than in the unexposed animals. The results suggest that a low-level inhalation exposure to HM, just like low-level exposure to PS, may lead to long-lasting disturbances in the CNS functions. The nonlinear concentration-effect relationship observed in the case of both TMB-s requires clarification in further studies.

Administration, Inhalation↗
PubMed1997

8-(N,N-diethylamino)-n-octyl-3,4,5-trimethoxybenzoate actions on calcium dynamics in cultured vascular smooth muscle cells.

AIM: To study 8-(N,N-Diethylamino)n-octyl-3,4,5-trimethoxybenzoate (TMB), a potent Ca(2+)-antagonist, actions on cellular calcium dynamics in vascular smooth muscle cell (VSMC) cultures. METHODS: A7r5 VSMC were cultured with Fura-2 measurements of intracellular Ca2+ concentration, [Ca2+]i. RESULTS: TMB reduced [Ca2+]i from control levels and blocked [Ca2+]i increase caused by norepinephrine (NE) and 2,5-di (t-butyl)-1,4-benzohydroquinone (BHQ). [Ca2+]i reduction by TMB was further enhanced by ryanodine. CONCLUSION: TMB is an effective agent for blocking the [Ca2+]i increase caused by NE and BHQ and for enhancing the [Ca2+]i reduction caused by ryanodine.

Animals↗
PubMed1998

8-(N,N-diethylamino)-n-octyl-3,4,5-trimethoxybenzoate reduced [Ca2+]i elevation induced by histamine, serotonin, and glutamate in cultured calf basilar artery smooth muscle cells.

AIM: To study the effects of 8-(N,N-diethylamino)-n-octyl-3,4,5- trimethoxybenzoate (TMB-8) on intracellular free calcium ([Ca2+]i) in cultured calf basilar artery smooth muscle cells. METHODS: [Ca2+]i was examined by a system of measurement of AR-CM-MIC, using Fura 2-AM as a fluorescent indicator. RESULTS: In the presence of extracellular Ca2+ 1.3 mmol.L-1, histamine (His), serotonin (5-HT), and sodium glutamate (Glu) markedly increased the [Ca2+]i which was attenuated by TMB-8. In Ca2+ free Hanks' solution containing egtazic acid 0.1 mmol.L-1, TMB-8 not only reduced the resting [Ca2+]i, but also inhibited the elevation of [Ca2+]i evoked by His and 5-HT. CONCLUSION: TMB-8 reduced the resting [Ca2+]i and attenuated His-, 5-HT-, and Glu-induced increases of [Ca2+]i in basilar artery smooth muscle cells.

Animals↗
PubMed1999

Plasma thrombomodulin levels in lung cancer patients.

BACKGROUND: Thrombomodulin (TM) is a glycoprotein and besides its anticoagulant property it is accepted as an onco developmental antigen. Considering these properties we hypothesised that active TMB might have a role in cancer cell behaviour. METHODS: We measured serum TMB levels by the enzyme immunoassay method in 40 patients with lung cancer and 20 healthy subjects. RESULTS: TMB levels were found as 54.6 +/- 11.5 in controls and 60.9 +/- 31.2 ng/ml in lung cancer patients TM levels were 59.4 +/- 24.2 ng/ml in 24 epidermoid carcinoma patients, 65 +/- 50.2 ng/ml in 10 small cell carcinoma patients and 60 +/- 18.4 ng/ml in 6 adenocarcinoma patients. Patients with stage 4 and distant metastasis had a value of 65 +/- 33.9 ng/ml. No significant differences were found between healthy subjects and cancer patients. Also the differences between 3 groups of patients were insignificant. CONCLUSIONS: It was concluded that serum TMB levels could not be accepted as a tumour marker in lung cancer patients.

Adult↗
PubMed2000

[The UV-Vis spectrographic and electrochemical study on the beta-cyclodextrin inclusion compound of 3,3',5,5'-tetramethylbenzidine].

This paper reports the results of UV-Vis spectrographic and electrochemical studying on the beta-cyclodextrin inclusion compound of 3,3',5,5'-tetramethylbenzidine (TMB). The molecules of TMB show better redox performance after they were included in the cavities of beta-cyclodextrin, especially while there were the redox enzyme. The composition of oxidization product in the inclusion compound is more single. The results were also revealed by the obviously increasing of voltammetrical current when this inclusion compound was modified on the electrode surface. It is reasonable to conclude that the formation of TMB-beta-cyclodextrin inclusion compound would enhance the sensitivity of those analytical methods based on the redox reaction of TMB.

Benzidines↗
PubMed2005

Calcium signaling is involved in ethanol-induced volume decrease and gap junction closure in cultured rat gastric mucosal cells.

Ethanol is a well-established "barrier breaker" in gastric mucosa, but its detailed effects at the cellular level remain unclear. We have previously shown that the intracellular free calcium concentration is increased, gap junctions are closed, and cell volume is decreased after exposure to 5% (v/v) ethanol in primarily cultured rabbit gastric epithelial cells. Rat gastric mucosal (RGM) cells were grown to confluence on a coverslip or on a filter membrane. Gap junctional diffusion was measured in 5-carboxyfluorescein-loaded cells by bleaching a small area with a laser and measuring the recovery with confocal microscope. Intracellular calcium was measured spectrofluorometrically in fura-2-loaded cells. For cell volume measurements the cell monolayer was loaded with calcein and imaged along the Z-axis with a confocal microscope. The changes in fluorescence intensity were intercepted as a measure of cell volume change. TMB-8 was used to inhibit intracellular calcium release and lanthanum to block plasma membrane calcium selective ion channels, while BABTA served as an intracellular calcium chelating agent. Results showed that ethanol (7.5%, v/v) exposure increased intracellular calcium from 69 +/- 7 to 142 +/- 11 nM (N = 5; P < 0.05), decreased cell volume by -23 +/- 5% (N = 8; P < 0.05), and induced gap junction closure (fluorescence recovery from 37 +/- 9 to 15 +/- 3%; N = 6; P < 0.05). A serosal potassium channel blocker, quinine, almost completely prevented the ethanol-induced cell volume decrease (from -23 +/- 5 to -3 +/- 3%), suggesting that opening of basolateral potassium channels underlies cell shrinkage. BABTA inhibited completely (from 35 +/- 3 to 39 +/- 4 nM; N = 6; P < 0.05), and TMB-8 + lanthanum partially (from 60 +/- 6 to 92 +/- 12 nM; N = 6; P < 0.05), the ethanol-induced intracellular calcium increase. BABTA also abolished the ethanol-induced volume decrease (from -23 +/- 5 to 1 +/- 4%; N = 6; P < 0.05), while TMB-8 + lanthanum had a lesser effect on it (from -23 +/- 5 to -11 +/- 3%; N = 9; P < 0.05). They also abolished the closure of gap junctions induced by ethanol (fluorescence recovery, 38 +/- 5% for BABTA and 30 +/- 4% for TMB-8 + lanthanum). We conclude that luminal ethanol opens basolateral calcium-dependent potassium selective channels with resultant shrinkage of the cells and blocks the intercellular gap junctions. These actions are mediated by intracellular calcium signaling.

Animals↗
PubMedDate not supplied

[Characterization of peroxidase-catalyzed oxidation of chromogenic substrates by tetrazole and its 5-substituted derivatives].

Peroxidase-catalyzed oxidation of 2,2-azino-di(3-ethyl-benzthiazolydine-6-sulfonic acid) (ABTS) and 3,3',5,5'-tetramethylbenzidine (TMB) is activated by tetrazole and its 5-substituted derivatives--5-amino-(AmT), 5-methyl- (MeT), 5-phenyl- (PhT), and 5-CF3- (CF3-T) tetrazoles. In phosphate-citrate or phosphate buffer (pH 6.4 or 7.2; 20 degrees C), the activating effect of tetrazoles on TMB and ABTS oxidation decreased in the series AmT > MeT > T > PhT > CF3-T and T > AmT > MeT > PhT, respectively. The (coefficient) degree of activation (alpha), expressed in M(-1), determined for both substrates and all activators, depended on substrate type, buffer nature, and pH (it increased as pH increased from 6.4 to 7.2). For TMB oxidation, good correlation between lgalpha and the Hammet constants sigma(meta) for m-substituents in the benzene series NH2, CH3, C6H5, and CF3 was found. It is suggested that AmT, MeT, and T can be used as activators of peroxidase-catalyzed oxidation of TMB and ABTS, as well as in designing peroxidase-based biosensors.

Enzyme Activation↗
PubMedDate not supplied

[Interaction of tropoxin and its molecular fragments tropan and 3,4,5-trimethoxybenzoate with serotonin receptors of cortical neurons in the rat brain (a microionophoretic study)].

The effects of the antimigraine drug tropoxin and its main molecular fragments - tropan and 3,4,5-trimetoxybenzoate (TMB) - on the serotonin sensitivity of postsynaptic neuronal membrane in rat brain sensorimotor area has been studied using a microionophoretic (MIP) technique. All the three substances significantly reduce the excitatory neuronal response to serotonin, which is manifested by an increase in the rate of the spontaneous action potentials. With respect to the antiserotonin effect, the substances can be arranged in the following order: tropoxin > tropan > TMB. The sum of the effects of tropan and TMB (for both simultaneous and separate action upon the target cells) was significantly lower than the effect of tropoxin in all doses (MIP currents). It is concluded that a pronounced antiserotonin effect of tropoxin is produced only provided that the entire molecular configuration is retained. Tropan and TMB, being tropoxin metabolites, are probably capable of prolonging the antimigraine action upon the decay of tropoxin in the organism. A relationship between the structure and action of serotonin receptor blockers of the tropan series is discussed.

Animals↗
PubMed1989

Interaction of 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride, ryanodine and procaine with muscarinic cholinergic M2 receptor sites in smooth muscle.

We have characterized muscarinic cholinergic receptor sites and interaction of various modulators of intracellular Ca mobilization, such as 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8), ryanodine, procaine and related drugs with the receptor sites, using a binding assay method with [3H]quinuclidinyl benzilate [( 3H]QNB) in guinea pig tenia cecum membrane fraction. [3H]QNB bound to a single population of sites, and the binding profile of pirenzepine suggest that the receptor sites are probably the M2 type. All the test drugs examined except for ryanodine displaced the [3H]QNB binding, and the slope factors were not different from unity. Affinities of these drugs were comparable to the concentrations usually used to modulate intracellular Ca mobilization. A Scatchard plot of [3H]QNB binding in the presence of TMB-8 or procaine showed that the apparent dissociation constant for [3H]QNB was increased without change in maximum binding. Neither TMB-8 nor procaine had any effect on the rate of dissociation of [3H]QNB from the steady-state complex. These results suggest that TMB-8 and procaine, and possibly other drugs, may interact directly with the muscarinic cholinergic M2 receptor sites in a competitive manner. In contrast, ryanodine had no effect on the [3H]QNB binding up to at least 100 microM. No interaction of ryanodine with M2 receptor sites lends a further support that the drug could be a useful probe for studying intracellular Ca mobilization.

Alkaloids↗
PubMed1985

[Cardiac and arterial causes of transient monocular blindness].

It has been accepted that transient monocular blindness (TMB) is highly suggestive of an ipsilateral carotid artery lesion in patients with arterial risk factors. We confirmed this in 55 patients, who had an internal carotid artery severe stenosis, occlusion or ulceration on angiography in more than 50 per cent of the cases. However, 12-lead-ECG, 2 D--echocardiography and Holter monitoring also showed a potential cardiac source of emboli in 22 per cent of the patients. Most of these patients (83 per cent) also had an appropriate arterial lesion, and the exact cause of the episodes of TMB remained undetermined. Our study shows that every fourth of fifth patient with TMB may have a potential cardiac source of emboli, the detection of which could alter the management. Systematic non-invasive cardiac investigations are warranted, especially in TMB patients with known heart disease.

Adult↗